a transcriptional co-regulatory protein. Proposed to mediate activation of the JNK pathway and apoptosis via ASK1 in response to signaling from FAS and TGF-betaR2. Glucose deprivation activates the ASK1-SEK1-JNK1-HIPK1 pathway, relocalizing Daxx from the nucleus to the cytoplasm, where Daxx binds to ASK1, and subsequently leads to ASK1 oligomerization. Interaction with HSP27 may prevent interaction with TGF-betaR2 and ASK1 and block DAXX-mediated apoptosis. Seems to act as a transcriptional co- repressor and inhibits PAX3 and ETS1 through direct protein- protein interaction. Its transcription repressor activity is modulated by recruiting it to subnuclear compartments like the nucleolus or PML/POD/ND10 nuclear bodies through interactions with MCSR1 and PML, respectively. Two alternatively spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Nuclear receptor co-regulator; Transcription, coactivator/corepressor
Molecular Function: protein binding; protein homodimerization activity; enzyme binding; androgen receptor binding; p53 binding; heat shock protein binding; ubiquitin protein ligase binding; receptor signaling protein activity; protein N-terminus binding; transcription factor binding
Biological Process: cytokinesis after mitosis; induction of apoptosis via death domain receptors; regulation of transcription, DNA-dependent; transcription, DNA-dependent; apoptosis; regulation of protein ubiquitination; virus-host interaction; androgen receptor signaling pathway; negative regulation of transcription, DNA-dependent; activation of JNK activity
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.